The candidate's background is in injury biomechanics, specifically in the passive material properties of soft tissues. His goal is to establish an independent research career in trauma biomechanics with particular focus on in-vivo and in-vitro models and to relate the effects of trauma at the cellular level to the macroscopic outcomes. In short-term, the candidate will enhance his knowledge of cardiovascular physiopathoogy and will develop an experimental and computational research program to study the mechanisms of traumatic arterial injuries that occur in automotive accidents. The candidate will be mentored jointly by senior faculty members of bioengineering and vascular surgery. The progress of candidate's work will also be evaluated semiannually by a 4-member advisory board. The research plan addresses the problem of traumatic aortic rupture (TAR) that is a leading cause of fatality in motor vehicle accidents. The mechanisms that have been proposed for TAR are speculative and inconclusive. The proposed research plan has three specific aims. In Specific Aim 1 an animal model of TAR will be developed which consists of porcine aorta positioned in a physical model of human thorax made of clear synthetic materials. The model will be mounted on a high speed impact system that will replicate decelerations and local crushing that are experienced by thoracic aorta in car crashes. The goal will be to generate TAR in different deceleration directions and local crush patterns. In Specific Aim 2 the material and failure properties of aorta layers will be determined by conducting a series tension, compression, and indentation tests on intact and dissected layers. The goal will be to develop a mathematical model of aorta that can predict large deformation and rupture considering the microstructural architecture. In Specific Aim 3 a Finite Element (FE) model of the experimental setup of Aim 1 will be developed. The results of Aim 2 and blood-wall interaction will be implemented in this model. The deformation, pressure, and rupture measured experimentally will be used to validate the model. In Specific Aim 4 the hypothesis that the local mechanism of TAR is local principal strain exceeding a certain threshold will be evaluated using the models developed in Aims 1, 2, 3. The risk functions that would relate TAR to global crash parameters will be derived. Relevance: This project will help to better understand the underlying mechanisms that cause traumatic rupture in aorta and how the risk of this major injury can be reduced. (End of Abstract)